Metabolism of malonaldehyde in vivo and in vitro.
The metabolism of malonaldehyde (MA) was investigated in vivo using male Wistar rats and in vitro using rat liver mitochondria. Twelve hr after intubation with [1,3-14C] MA, 60-70%, 5-15% and 9-17% of administered radioactivity was recovered in expired CO2, feces and urine, respectively. In rats intubated with [1,2-14C) acetate, the corresponding values were 68-82%, 1-2% and 2.3%. 14CO2 evolution was initially slower after 14C-MA administration than after 14C-acetate administration and more radioactivity was excreted in the feces and urine. In vitro experiments using [1,3-14C] MA showed that MA is metabolized primarily in the mitochondria via reactions involving O2 utilization and 14CO2 production. The apparent Km and Vmax were 0.5 mM and 9.3 nmol/min/mg protein for O2 uptake, respectively, and 2.0 mM and 2.4 nmol/min/mg protein for 14CO2 production. Addition of malonic acid to mitochondrial incubates at concentrations inhibitory to succinate dehydrogenase did not affect MA-induced O2 uptake but enhanced 14CO2 production from 14C-MA. 14C-Acetate appeared to be the major accumulating metabolite in rat liver mitochondrial preparations following a 120-min incubation with 14C-MA. A probable biochemical route for MA metabolism involves oxidation of MA by mitochondrial aldehyde dehydrogenase followed by decarboxylation to produce CO2 and acetate.
D000085:Acetates / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D007700:Kinetics; D008297:Male; D008314:Malonates / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism; D008956:Models, Chemical; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013997:Time Factors
D000085:Acetates; D008314:Malonates; D002245:Carbon Dioxide; D008315:Malondialdehyde; D013385:Succinate Dehydrogenase